The present invention relates to a device for controlling the electrical activity of the heart. More particularly, the invention relates to a device and a method for the cessation and/or prevention of malignant cardiac arrhythmias.
Sudden cardiac death is heralded by the abrupt loss of consciousness within a short period of time (usually not more than one hour) after the onset of acute symptoms. Estimates indicate nearly 400,000 sudden cardiac deaths annually for the USA only. Malignant cardiac arrhythmias such as Ventricular Tachycardia (VT) and Ventricular Fibrillation/Flutter (VF) are included in one category that is a major cause of sudden death usually associated with a diseased human heart. When VT/VF occurs, the patient may die within a few minutes without immediate intensive care. The conventional treatment which is normally given to the patient in the hospital is delivering a high energy electrical shock to the heart, usually from 200-400 Joules (J). The shock is applied between two electrodes (paddles) of an external defibrillator attached to the patient""s chest. This shock resets the electrical activity of the heart, so as to enable a new natural initiation of normal electrical activity. However, these relatively high energy levels may cause heart tissue damage, especially in cases of multiple shocks, and in the long run may be dangerous, particularly in patients with a diseased heart. In addition, due to the severe pain caused by high energy impulses plus possible harm by severe contraction of the body musculature, high energy cardiac shocks are usually administered to unconscious or anesthetized patients.
The most effective method for appropriate management of patients who suffer from VT/VF is by employing an implantable cardiovertor defibrillator (ICD) device. This ICD applies electrical shocks directly to the heart when the device itself diagnoses VT/VF. These directly applied shocks are of much lower energy than those of the external defibrillator (normally ranging between 10 and 30 J), but, even this relatively low-energy application is very painful and may be harmful to the heart muscle in the long run.
Normal heart activity is controlled by impulses, which are generated at the sino-atrial node, and propagate from cell to cell through the special conduction system and myocardium, thereby causing an ordered contraction. Excitation in normal heart tissue is followed and terminated by refractoriness. This important feature of the heart provides it with electrical stability, so that abnormal excitation waves cannot propagate during the refractory period.
The exact mechanisms of malignant cardiac arrhythmias are not completely clear. In most cases it is assumed that they result from a xe2x80x9csourcexe2x80x9d in the heart, around which a closed electrical circuit is generated, thereby forming a xe2x80x9creentryxe2x80x9d path in the myocardium. There are two main approaches for management of malignant cardiac arrhythmia: pharmacological and non-pharmacological. The former generally can prevent and treat malignant cardiac arrhythmias, however its clinical effect for preventing sudden cardiac death is relatively low. In the non-pharmacological approach, malignant arrhythmias such as VT or VF may be treated by electrical shock (defibrillation/cardioversion) and can be prevented by ablation (annihilation) of part of the re-entry pathway or of the xe2x80x9csourcexe2x80x9d of abnormal electrical activity.
All the methods described above have not yet provided complete satisfactory solutions to the appropriate overall management of malignant cardiac arrhythmias.
It is an object of the present invention to provide a method and a device for the management of malignant cardiac arrhythmia, which overcomes the drawbacks of the prior art.
It is another object of the present invention to provide a method and a device for the management of malignant arrhythmia, using very low energy impulses.
It is still another object of the present invention to provide a method and a device for the management of malignant arrhythmia without immediate or delayed negative effects on the patient""s myocardium.
It is still another object of the present invention to provide a method and a device for the management of VT/VF, the use of which is not painful.
Other objects and advantages of the invention will become apparent as the description proceeds.
While the device of the invention is designated herein as a xe2x80x9cdevice for the cancellation of unwanted excitation wavesxe2x80x9d, it should be understood that the xe2x80x9cunwanted excitation wavesxe2x80x9d are those causing cardiac tachyarrhythmias, and the use of the device to prevent or terminate these waves or other related pathological phenomena is included in the invention.
The device of this invention comprises the means for canceling unwanted excitation waves that propagate in an excitable tissue, by generating an excitation wave that spreads preferentially in a desirable direction. The excitation wave, also termed Device-Generated Excitation Wave (DGEW) may be directed opposite to that of the unwanted excitation wave and could cancel it or reduce it to such a magnitude that it ceases to propagate and decays. Said means for controlling the spread of the DGEW comprises two bipolar stimulating electrodes, which are adapted to be inserted into the excitable tissue at two different locations. Each stimulation electrode is fed by a power supply. Each stimulation electrode preferably comprises a pair of conducting needles, each of which comprises a relatively sharp tip at its distal end, and the proximal end of each such needle is connected to the contact of said power supply. When in use, each needle of the pair has an opposite polarity and they form a closed conducting current path through the underlying excitable tissue. The proximal end of each opposite-polarity needle is connected to a different contact of the corresponding power supply. When reference is made herein to a first and a second power supply, one for each pair of opposite-polarity stimulation electrodes, this should be understood to signify that the means for independently feeding power to each needle pair is provided, whether through two separate power sources or through a single power source with two separately controllable outputs. The device further comprises a first and second control circuitry, respectively, for generating the required amplitude and duration of the voltage applied between the respective needles. This forces a clamped current impulse to flow between the needles of each stimulation electrode. While reference is made to a first and second control circuitry, they can and generally are included in a single electronic circuit.
The first power supply, which drives the first stimulation electrode, is set to generate a first current stimulus, S1, with magnitude that is lower than the threshold level of the excitable tissue. Hereinafter, the term xe2x80x9cthreshold leverxe2x80x9d is used to describe the current stimulus magnitude, at which the tissue becomes excited and the DGEW starts to propagate actively throughout the tissue. Stimuli below the threshold level cannot elicit an actively propagating wave along the tissue and decays over space and time. The second power supply, which drives the second stimulation electrode, is set to generate a second current stimulus, S2, with magnitude that is higher than the threshold level of the excitable tissue. The terms xe2x80x9cfirst and secondxe2x80x9d current stimuli do not indicate timing, but indicate that the stimuli are delivered by the first and the second stimulating electrode, respectively.
The combination of S1 and S2 generates a DGEW, which spreads preferentially in one direction, that is controllable and can be made to be opposing to the unwanted wave. The delay between S1 and S2 is set by a timing circuitry to compensate for any change in the relative location between the two stimulation electrodes that may be desired.
Preferably, the distance between the two stimulating electrodes is adjusted to be approximately between 0.1 and 1.5 mm. Preferably, the distal end of the needle of each stimulating electrode consists of a 100
82 m long exposed metal cone, with a 10 xcexcm diameter tip. The needle segment connecting between its proximal end and its distal end is insulated, so as to limit current impulse generation to the vicinity of the distal end. Preferably, the magnitude of the second current impulse, S2, is between 1.25 and 1.5 times the threshold level of the excitable tissue. Preferably, the delay between the two impulses (which is equal to timing of S2 minus timing of S1) is between xe2x88x9210 mSec and +5 mSec, and the duration of each current impulse is approximately 100 xcexcs. The propagation direction of the remaining DGEW can be switched by increasing the magnitude of the first stimulus, S1, above the threshold level of the excitable tissue, and decreasing the magnitude of the second stimulus, S2, below the threshold level of the excitable tissue. The distance between the two stimulating electrodes is set so that the two impulses interact with each other only in one desired direction, while preventing interaction in the opposite direction.
Preferably, the device comprises a detector circuitry, linked to the aforesaid first and second control circuits of each stimulation electrode and to the timing circuitry, for detecting unwanted excitation waves in the excitable tissue which are above the threshold level. The device is operated automatically whenever an unwanted wave is detected. In response, an opposing impulse wave is generated. Said wave interferes with the unwanted one and reduces its magnitude below the threshold level, thereby causing the unwanted wave to decay. The device can reside outside of the excitable tissue with only the electrodes implanted within the tissue. Alternatively, the whole device can be implanted in the excitable tissue. The invention further comprises the use of the aforesaid device for suppressing malignant cardiac arrhythmias.
The present invention is also directed to a method for medical treatment and suppression of malignant cardiac arrhythmias in patients, resulting from unwanted excitation waves generated and sustained in closed re-entry conductive paths in the heart of the patient, by generating unidirectional excitation waves for interacting with the unwanted excitation waves and canceling them. The method enables medical treatment and suppression of malignant cardiac arrhythmias in patients, resulting from unwanted excitation wave. Low-energy, asymmetrical excitation impulses are generated in two different locations in the myocardium. The first impulse has a magnitude below the threshold level of the myocardium tissue, and the second impulse has magnitude above the threshold level. The distance between the two locations, and the time of the generation of the impulses is determined, so that the passive electric depolarization generated by the first excitation impulse interacts with the propagating action potential generated by the second excitation impulse, thereby preventing the spreading of excitation wave in an undesirable directions. The remaining unidirectional excitation wave cancels the unwanted wave in its re-entry path. Preferably, one excitation impulse is generated with a delay in respect to the other excitation impulse. Both excitation impulses may also be generated concurrently.
Let us call the impulses that travel in one direction xe2x80x9cd impulsesxe2x80x9d and those that travel in the opposite direction xe2x80x9cs impulsesxe2x80x9d and let us say that the unwanted impulse is a xe2x80x9cd impulsexe2x80x9d. Then one applies two electrodes A and B, wherein electrode A generates two impulses Ad and As above the threshold and B generates two impulses Bd and Bs below the threshold. Impulse As will interact with the unwanted impulse and these two impulses will cancel each other. Impulse Bd will decay. The distance between the electrodes and the timing of impulse generation are either such that impulse Ad interacts with impulse Bs before this decays, and the interaction generates a residual impulse that is below the threshold and therefore decays. However, alternatively, if the two electrodes are sufficiently close to one another, no impulses are generated between them, viz. there are no impulses Ad and Bs. In either case, no impulse thus remains to propagate through the heart tissue.
Therefore, the method comprises:
axe2x80x94generating, by means of a first electrode, a first impulse above the threshold that propagates opposite to the unwanted impulse, whereby when it meets said unwanted impulse, the two impulses cancel one another;
bxe2x80x94generating, by means of a second electrode a second impulse below the threshold, that propagates in the same direction as the unwanted impulse and decays; and
cxe2x80x94choosing the distance between said electrodes and the timing of the impulse generation in such a way that the first electrode generates a third impulse above the threshold that propagates in a direction opposite to that of said first impulse threshold, while the second electrode generates a fourth impulse below the threshold that propagates in a direction opposite to that of said second impulse, whereby said third and fourth impulse meet and their interaction generates a residual impulse that is below the threshold and decays;
dxe2x80x94provided that if said distance is small enough, no third and no fourth impulse are generated.
The present invention also provides a method for localizing the pathological tissue (or pathways) that are responsible for arrhythmias. The location of the re-entry path of the unwanted excitation wave are identified from the direction of the remaining sub-impulse when this latter cancels the unwanted excitation wave, and destructive energy is delivered to the identified location.
In the following description, it is assumed that the stimulation electrodes are positive; however, this is not to be construed as an absolute, and they could be negative.